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22 Cards in this Set
- Front
- Back
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How many parathyroid glands are there? Where are they located? |
- 4 glands - Located on the posterior upper and lower poles of the thyroid gland |
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What do the parathyroid glands do? |
- They secrete parathyroid hormone (PTH), a polypeptide hormone, which regulates plasma calcium and concentrations - PTH is also secreted during hyperphosphatemia and acute hypomagnesemia |
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What are normal plasma concentration levels of calcium? What are normal total serum calcium levels? What are normal ionized calcium levels? |
- Plasma: 4.5- 5.5 mEq/L - Total serum: 8.6- 10.6 mg/dL - Ionized: 4.7- 5.2 mg/dL |
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Why is ionized calcium important? What are the effects of it? |
- Ionized Ca+ is the physiologic active form of Ca+. It exerts physiologic effects such as: * Platelet aggregation * Blood coagulation * Muscle contraction * Neurotransmission * Bone formation * Cell division * Other aspects of cell function "Peanut Butter May Never Be a Cool Option" |
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How does PTH increase plasma calcium levels? How does it decrease serum phosphate levels? |
- It promotes movement of Ca+ across 3 interfaces: Bone, renal tubules & GI tract * Promotes bone resorption * Limits renal excretion at the distal convoluted tubule * Indirectly enhances GI absorption by its effect on vitamin D metabolism - Decreases serum phosphate by increasing renal excretion at the proximal convoluted tubule |
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How much calcium is stored in the bones? |
99% which means the bones are a large reservoir that can store or release Ca+ as needed |
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How does a decrease in albumin affect ionized serum calcium? |
- Changes in serum calcium are parallel to changes in serum albumin. - A decrease in serum albumin decreases total serum calcium levels because ionized serum Ca+ is dependent on plasma albumin concentration. |
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How does pH affect ionized serum calcium levels? |
- Alkalosis decreases ionized Ca+ by increasing protein- Ca+ binding - Acidosis increases ionized Ca+ by decreasing protein-Ca+ binding |
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Which electrolytes does vitamin D (cholecalciferol) alter? |
- Vitamin D increases plasma Ca+, Mg+, and PO4 ion concentrations by promoting their absorption across the intestinal epithelium to the extracellular fluid |
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What is the difference between osteoclasts and osteoblasts? |
- When ionized serum calcium is low, PTH from the parathyroid is released to activate and proliferate osteoclasts - Osteoclasts are bone-destroying cells that increase serum calcium levels. - In contrast, when ionized serum calcium is high, calcitonin is released from the thyroid. - Calcitonin signals osteoblasts which are bone-forming cells and they restore the calcium to the bone. |
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What is hyperparathyroidism? What is the difference between primary, secondary, and ectopic hyperparathyroidism? |
- Presence of elevated serum PTH despite high serum calcium levels - Primary: Caused by adenoma (90%), carcinoma, or hyperplasia of the parathyroid gland - Secondary: Adaptive response to hypocalcemia from diseases such as renal failure or intestinal malabsorption syndromes - Ectopic: Production of PTH by tumors outside the parathyroid gland (rare) |
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What does "stones, bones, and groans" mean? |
- This refers to the renal, skeletal, and GI features of advanced hyperparathyroidism. - Renal (stones) * Renal stones * Renal failure * Impaired concentrating abilities * Hyperchloremic metabolic acidosis * Polyuria * Polydipsia, * Dehydration - Skeletal (bones) * Muscle weakness * Osteoporosis - GI (groans) * Ileus * N/V * PUD * Pancreatitis |
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What are the cardiovascular changes seen in hyperparathyroidism? What are the neurological changes? |
- Cardiovascular * HTN * Ventricular dysrhythmias * Shortened QT-intervals * PR-interval maybe prolonged - Neurological * Mental status changes - Delirium - Psychosis - Coma |
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What is treatment for hyperparathyroidism? |
- Medical management first * NS @ 150 ml/hr * Loop diuretics * Goal is for daily u.o. = 3-5 L * Biphophonates IV for severe hypercalcemia * Hemodialysis * Calcitonin (transient effect) - Surgical removal * Remove diseased or abnormal part of parathyroid glands * Remove all 4 glands if parathyroid hyperplasia
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What are preoperative considerations for hyperparathyroidism? |
- Maintain adequate hydration and u.o. - Be careful with positioning because these pts. are prone to pathologic fractures - Minimal preoperative sedation because of somnolence |
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What are intraoperative considerations for hyperparathyroidism? |
- Avoid hypoventilaion = Increases ionized Ca+ - Avoid ketamine= underlying psych issues r/t hypercalcemia - Take caution with sevoflurane= Underlying kidney issues - Take caution with muscle relaxants= Unpredictable responses, start slow and then titrate in - Monitor EKG * dysrhythmias may be present |
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What are postoperative considerations for hyperparathyroidism? |
- Parathyroidectomy * Same as subtotal thyroidectomy * Hypocalcemic tetany - Methylene blue * Used intratoperatively to find parathyroid tissue * Can cause a spurious decrease in SaO2 |
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What is hypoparathyroidism? What are causes of hypoparathyroidism? |
- Secretion of PTH is absent or deficient or peripheral tissues are resistant to effects of the hormone * Pseudohypoparathyroidism * Hypomagnesemia * Chronic renal failure- most common cause * Malabsorption * Anticonvulsive therapy (phenytoin) * Osteoblastic metastases * Acute pancreatitis - Common complication of parathyroidectomy or inadvertent removal of parathyroids during thyroidectomy - Idiopathic (DiGeorge's syndrome) |
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What is pseudoparathyroidism? |
-Occurs when the PTH is released normally, but the kidneys are unable to respond to it. - Associated with mental retardation, basal ganglia calcification, obesity, decreased height, and short metacarpals and metatarsal bones. |
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What are acute clinical manifestations of hypoparathyroidism? What are chronic signs? |
- Acute * Perioral parasthesias * Restlessness * Neuromuscular irritability * + Chvostek sign or Trousseau sign * Neuromuscular irritability (laryngospasm, inspiratory stridor) - Chronic * CV: Hypotension, CHF, prolonged QT-interval * Musculoskeletal: Muscle cramps, weakness * Neurologic: Tetany, seizures, lethargy, cerebration deficits, mental status change (dementia, depression, psychosis) |
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What is the treatment for acute hypocalcemia? |
- Infusion of Calcium if symptomatic hypocalcemia * 10 ml of 10% Calcium gluconate * 10 ml of 10% CaCl -Theoretically CaCl is supposed to be 3x more potent than Calcium gluconate and should only be administered through a central line, although the book does not attest to this - Oral calcium and vitamin D for treatment of hypoparathyroidism but not symptomatic hypocalcemia - Respiratory or metabolic alkalosis should be normalized - Thiazide diuretics may be helpful as they result in sodium depletion without the loss of potassium which tends to increase calcium levels. |
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How is anesthesia managed for a hypoparathyroid pt? |
- Prevent further decrease in Ca+ * Avoid hyperventilation & alkalosis * Avoid sodium bicarbonate - Avoid anesthetics that depress the myocardium * Watch EKG for prolonged QT - Avoid rapid infusion of citrate-containing blood products * Decrease Ca+ levels - Avoid vigorous diuresis - Avoid use of 5% albumin solutions * Binds and lowers ionized Ca+ - Monitor for coagulopathy - May be sensitive to muscle relaxants * Start slow and low and then titrate in |
